Metabolic control of respiratory neuronal activity and the accompanying changes in breathing movements of the rabbit

Summary

The property of the neuronal membrane to be permeable to metabolic modifiers of two regulatory enzymes has been utilized to manipulate the spike activity of inspiratory (I) and expiratory-inspiratory (EI) neurons of the bulbar respiratory centre. The neurons have been classified according to their response to lung distension or collapse (α- or β-type) and to hyperventilation (tonic firing denoted by “+”, cessation of activity by “−”). Using extracellular microelectrodes for single unit recording, the medulla oblongata was superfused with a metabolite-containing CSF. The various neuronal sub-types exhibited a differential activating or inhibitory response to one or several metabolic effectors. For example Iα+ units were activated by 5 mM glucose-6-phosphate (G-6-P) and 3.5 mM 3-phosphoglycerate (3-PGA), which both inhibited Iβ+ neurons, while 5 mM AMP inhibited Iα+ much more strongly than Iβ+ cells. The spike density of Iα− and Iβ− neurons was increased in the presence of 2.5 mM fructose-6-phosphate and 3.5–5 mM AMP, but became reduced by G-6-P. In contrast, 3 mM fructose-1,6-diphosphate and 5 mM 3-PGA activated the Iα− but inhibited the Iβ− neurons. The EIβ units were characteristically activated by 10 mM citrate, which inhibited all I-type neurons. Activations of the Iα and Iβ neurons led to an accelerated respiratory rate and a higher tidal volume, while the opposite was true for EIβ neurons. Intravenous injection of metabolites could not duplicate the striking effects under local applications.

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